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目的:研究心肌肥厚和心力衰竭时左心室收缩力及钙瞬变的变化。方法:采用主动脉缩窄术构建压力负荷型心衰小鼠模型及心肌肥厚小鼠模型,小动物超声机测量小鼠心室壁厚度及射血分数,Langendorff灌流术分离小鼠左心室心肌细胞,高速CCD摄像机系统和双激发荧光倍增系统同步测量左心室心肌细胞肌小节收缩舒张功能和胞内钙瞬变。结果:与假手术组相比,肥厚小鼠心室壁明显增厚,胞质基础钙浓度、钙瞬变振幅增高,钙瞬变达峰时间、恢复时间和肌小节舒张时间明显延长,肌小节初长度缩短;心衰组小鼠心腔扩大,射血分数(EF)、钙瞬变峰值、峰高、达峰时间及胞质内钙恢复的速度明显下降,肌小节初始长度显著缩短,收缩幅度下降,静息期基础钙浓度显著上升,收缩及舒张时间均明显延长。结论:在心力衰竭的发展过程中,随着心脏结构的改变,心肌细胞对胞内钙的释放和回收能力均下降,使单个心肌细胞收缩无力、舒张时间延长,进而影响整个心脏的收缩舒张功能。改善心肌细胞钙循环可能在缓解心衰患者临床症状和改善预后方面起到关键作用。
Objective: To study the changes of left ventricular contractility and calcium transients during cardiac hypertrophy and heart failure. Methods: A rat model of stress-induced heart failure and hypertrophic myocardium were established by aortic constriction. The thickness and ejection fraction of ventricular wall were measured by using a small animal ultrasound machine. Left ventricular myocytes were isolated by Langendorff perfusion. High-speed CCD camera system and double-excited fluorescence doubler system synchronous measurement of left ventricular myocardial muscle contraction and diastolic function and intracellular calcium transients. Results: Compared with the sham-operated group, the ventricular wall of hypertrophied mice was significantly thicker, the cytoplasmic calcium concentration, the amplitude of calcium transient increase, the peak of calcium transient peak time, the recovery time and the relaxation time of myotubes were significantly prolonged, The length of shortening of cardiac muscle in heart failure rats increased, the ejection fraction (EF), peak of calcium transients, peak height, peak time and the rate of cytoplasmic calcium recovery decreased significantly, the initial length of muscle segments was significantly shortened, the amplitude of contraction Decreased, basal calcium concentration at rest increased significantly, systolic and diastolic time were significantly prolonged. CONCLUSION: During the development of heart failure, with the change of cardiac structure, the release and recovery of intracellular calcium by cardiomyocytes are decreased, weakening of single cardiomyocytes, prolonged diastole, and thus affecting the systolic and diastolic function of the whole heart . Improving calcium circulation in cardiomyocytes may play a key role in alleviating clinical symptoms and improving prognosis in patients with heart failure.